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Oncogene regulated by nutrients identified

April 13, 2015
Centro Nacional de Investigaciones Oncologicas (CNIO)
In response to nutrient excess, the MCRS1 protein acts as a 'switch' for mTOR, a protein that is altered in cancer, diabetes and disorders associated with aging. These results correlate with increased MCRS1 protein levels in samples taken from patients with colorectal cancer. Blocking this protein may prove to be an effective treatment for cancer or other diseases associated with mTOR alterations, researchers say.

Scientists from the Growth Factors, Nutrients and Cancer Group at the Spanish National Cancer Research Center (CNIO), led by Nabil Djouder, have discovered that the MCRS1 protein, in response to an excess of nutrients, induces an increase in the activity of mTOR (the mammalian/mechanistic Target of Rapamycin); a protein that is altered in human diseases such as cancer and diabetes, processes associated with aging, as well as in certain cardiovascular and neurodegenerative pathologies. The finding, published in the journal Developmental Cell, opens up new possibilities for the development of drugs that block MCRS1 to treat cancer and diabetes.

Under normal conditions, mTOR regulates essential cellular functions, such as protein synthesis and cell growth and proliferation. However, an overactive stimulation of mTOR in response to nutrients and growth factors --metabolic processes that are crucial in tumor biology-- leads to an increase in cell growth and proliferation.


CNIO researchers have now discovered how the MCRS1 protein --a protein associated with gene regulation and cell death processes-- is capable of activating mTOR, and thus, stimulate cell proliferation. In this way, in human colorectal cancer samples, a correlation was found between increased MCRS1 activity and tumours with a high proliferation rate, as well as with a worse prognosis of the disease.

"Although in our study we published the results obtained from these colorectal samples, we are also studying the relationship between this protein and diseases of the liver, the primary metabolic organ," explains Djouder.


The incidence of cancer and other related diseases has increased considerably in Western societies; this is partly due to an increased caloric intake and a more sedentary lifestyle. Therefore, unravelling the cellular processes that act in response to an excess of nutrients can contribute to achieve a better understanding of the biology of cancer and, consequently, is key to the fight against this disease.

"We will continue to study this gene using different genetically modified mouse models, where we can study what occurs when there is a gain- or loss-of-function. We are already obtaining interesting results, but further research is necessary."

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Materials provided by Centro Nacional de Investigaciones Oncologicas (CNIO). Note: Content may be edited for style and length.

Journal Reference:

  1. Mohamad-Ali Fawal, Marta Brandt, Nabil Djouder. MCRS1 Binds and Couples Rheb to Amino Acid-Dependent mTORC1 Activation. Developmental Cell, 2015; 33 (1): 67 DOI: 10.1016/j.devcel.2015.02.010

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Centro Nacional de Investigaciones Oncologicas (CNIO). "Oncogene regulated by nutrients identified." ScienceDaily. ScienceDaily, 13 April 2015. <>.
Centro Nacional de Investigaciones Oncologicas (CNIO). (2015, April 13). Oncogene regulated by nutrients identified. ScienceDaily. Retrieved December 10, 2023 from
Centro Nacional de Investigaciones Oncologicas (CNIO). "Oncogene regulated by nutrients identified." ScienceDaily. (accessed December 10, 2023).

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